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Bioelectronics is a hot research topic, yet an important tool, as it facilitates the creation of advanced medical devices that interact with biological systems to effectively diagnose, monitor and treat a broad spectrum of health conditions. Electrical stimulation (ES) is a pivotal technique in bioelectronics, offering a precise, non-pharmacological means to modulate and control biological processes across molecular, cellular, tissue, and organ levels. This method holds the potential to restore or enhance physiological functions compromised by diseases or injuries by integrating sophisticated electrical signals, device interfaces, and designs tailored to specific biological mechanisms. This review explains the mechanisms by which ES influences cellular behaviors, introduces the essential stimulation principles, discusses the performance requirements for optimal ES systems, and highlights the representative applications. From this review, we can realize the potential of ES based bioelectronics in therapy, regenerative medicine and rehabilitation engineering technologies, ranging from tissue engineering to neurological technologies, and the modulation of cardiovascular and cognitive functions. This review underscores the versatility of ES in various biomedical contexts and emphasizes the need to adapt to complex biological and clinical landscapes it addresses. [ABSTRACT FROM AUTHOR]

This article explores the potential of melatonin to mitigate circadian clock disturbances in mice with fibrosis and human hepatic stellate cells. The study found that treatment with carbon tetrachloride (CCl4) resulted in fibrosis and dysregulation of circadian clock genes in mice, but melatonin administration prevented these changes. Additionally, melatonin exposure upregulated clock gene expression in human hepatic stellate cells. These findings provide new insights into the molecular pathways involved in the protective effects of melatonin in liver fibrosis. [Extracted from the article]

MicroRNAs (miRs) are a group of small, 17–25 nucleotide, non-coding RNA that regulate gene expression at the post-transcriptional level. To date, little is known about the molecular signatures of regulatory interactions between miRs and apoptosis and oxidative stress in viral diseases. Lagovirus europaeus is a virus that causes severe disease in rabbits (Oryctolagus cuniculus) called Rabbit Hemorrhagic Disease (RHD) and belongs to the Caliciviridae family, Lagovirus genus. Within Lagovirus europaeus associated with RHD, two genotypes (GI.1 and GI.2) have been distinguished, and the GI.1 genotype includes four variants (GI.1a, GI.1b, GI.1c, and GI.1d). The study aimed to assess the expression of miRs and their target genes involved in apoptosis and oxidative stress, as well as their potential impact on the pathways during Lagovirus europaeus—two genotypes (GI.1 and GI.2) infection of different virulences in four tissues (liver, lung, kidneys, and spleen). The expression of miRs and target genes related to apoptosis and oxidative stress was determined using quantitative real-time PCR (qPCR). In this study, we evaluated the expression of miR-21 (PTEN, PDCD4), miR-16b (Bcl-2, CXCL10), miR-34a (p53, SIRT1), and miRs—related to oxidative stress—miR122 (Bach1) and miR-132 (Nfr-2). We also examined the biomarkers of both processes (Bax, Bax/Bcl-2 ratio, Caspase-3, PARP) and HO-I as biomarkers of oxidative stress. Our report is the first to present the regulatory effects of miRs on apoptosis and oxidative stress genes in rabbit infection with Lagovirus europaeus—two genotypes (GI.1 and GI.2) in four tissues (liver, lungs, kidneys, and spleen). The regulatory effect of miRs indicates that, on the one hand, miRs can intensify apoptosis (miR-16b, miR-34a) in the examined organs in response to a viral stimulus and, on the other hand, inhibit (miR-21), which in both cases may be a determinant of the pathogenesis of RHD and tissue damage. Biomarkers of the Bax and Bax/Bcl-2 ratio promote more intense apoptosis after infection with the Lagovirus europaeus GI.2 genotype. Our findings demonstrate that miR-122 and miR-132 regulate oxidative stress in the pathogenesis of RHD, which is associated with tissue damage. The HO-1 biomarker in the course of rabbit hemorrhagic disease indicates oxidative tissue damage. Our findings show that miR-21, miR-16b, and miR-34a regulate three apoptosis pathways. Meanwhile, miR-122 and miR-132 are involved in two oxidative stress pathways. [ABSTRACT FROM AUTHOR]

Rabbit Haemorrhagic Disease (RHD) is a severe disease caused by Lagovirus europaeus/GI.1 and GI.2. Immunological processes such as apoptosis are important factors involved in the pathogenesis of Rabbit Haemorrhagic Disease (RHD). The process of programmed cell death has been quite well characterized in infection with GI.1 strains, but apoptosis in infection with GI.2 strains has not been widely studied. This is particularly important as several studies have shown that significant differences in the host immune response are observed during infection with different strains of Lagovirus europaeus. In this study, we analyzed the gene expression, protein levels and activity of key apoptotic cell death factors in the spleen, kidney, lung, and heart of rabbits. As a result, we showed that there is a significant increase in caspase-3, Bax, Bcl2 and Bax/Bcl2 mRNA gene expression ratio in organs of infected animals. Our results show also increased levels of cleaved caspase-3, caspase-6 and PARP. Moreover, significant activity of caspase-3 was also detected. Our results indicate that caspase-3, caspase-6 and genes coding Bcl2 family proteins play a key role in the apoptotic response in Lagovirus europaeus/GI.2 infection in organs that are not the target of virus replication. [ABSTRACT FROM AUTHOR]

Copyright of Revista Colombiana de Investigaciones Agroindustriales is the property of Revista Colombiana de Investigaciones Agroindustriales del Centro Agropecuario Sena Buga and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Iraqi Journal of Agricultural Sciences is the property of Republic of Iraq Ministry of Higher Education & Scientific Research (MOHESR) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Some plant foods evolve defense mechanisms to protect themselves from predators by producing inherent chemicals as secondary metabolites such as cyanogenic glycosides, glycoalkaloids, glucosinolates, pyrrolizidine alkaloids, and lectins. These metabolites are beneficial for the plant itself but toxic to other organisms, including human beings. Some of these toxic chemicals are believed to have therapeutic benefits and are therefore used to protect against chronic health complications such as cancer. Inversely, short- and long-term exposure to significant amounts of these phytotoxins may end up with chronic irreversible negative health problems in important organ systems, and in severe cases, they can be carcinogenic and fatal. A systematic literature search of relevant published articles indexed in Google Scholar®, PubMed®, Scopus®, Springer Link®, Web of Science®, MDPI®, and ScienceDirect databases was used to obtain the necessary information. Various traditional and emerging food-processing techniques have been found to considerably reduce most of the toxicants in the food to their safest level. Despite their ability to preserve the nutritional value of processed foods, emerging food processing methods have limited application and accessibility in middle- and low-income countries. As a consequence, much more work is recommended on the implementation of emerging technologies, with additional scientific work on food processing methods that are effective against these naturally occurring plant food toxicants, particularly pyrrolizidine alkaloids. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases are the leading cause of death worldwide. The most common underlying pathologies of cardiovascular disorders are thromboembolic diseases. The antithrombotic therapy prevents the formation of thrombi or dissolves the previously constituted ones. However, it presents a high rate of accidents such as gastric bleeding and cerebrovascular embolisms. Thus, the use of herbal medicine has become a viable option for the treatment of such diseases. Reports of traditional Mayan and Nigerian medicine indicate that the Cnidoscolus aconitifolius (Mill.) I.M. Johnst, knowed as Chaya by Mayas in Yucatán, is used as a blood thinner. Currently, there are limited scientific reports that support the antithrombotic activity of the chaya, among which its cardioprotective, anticoagulant and fibrinolytic effect has been reported. However, the exact mechanism by which the chaya exerts these effects is not yet known. Due to the ethnobotanical reports of traditional medicine and existing scientific studies, it is possible to suggest that chaya extracts exert a biological effect on various platelet, coagulant and fibrinolytic enzymes of the blood hemostatic system. This review will analyze the content of secondary metabolites present in Cnidoscolus aconitifolius (Mill.) I.M. Johnst leaf extracts, in order to propose the possible antithrombotic mechanisms of chaya. [ABSTRACT FROM AUTHOR]

Due to the great variations in altitude, humidity, hours of exposure to the sun, chemical and microbiological composition of the soil, the Andean and Amazon regions of Peru have a great diversity of microclimates, thus allowing the development of a wide variety of species of plants producing edible fruits. In addition to their nutritional value, these fruits are characterized by the presence of high levels of compounds beneficial to health, particularly polyphenols, such as flavonoids, lignans, phenolic acids, and stilbenes, and natural pigments, such as betalains. Several studies have shown that these compounds have antioxidant, antimicrobial, antitumor, and immunogenic activities and, therefore, can contribute to the prevention of diseases such as cancer, diabetes, and hypertension. Given the accumulated evidence, we believe that the consumption of fresh fruits from these regions, or even those preserved through industrial processes that maintain their properties, should be strongly encouraged. This manuscript aims to present and discuss the literature relevant to the benefits of consuming fruits from the Amazon and Andean regions of Peru for health maintenance. [ABSTRACT FROM AUTHOR]

Acetaminophen (APAP) overdose is one of the leading causes of acute liver damage. Given N-acetylcysteine (NAC) and melatonin (MLT) both have an attenuated value for APAP-induced liver toxification, where an optimized integrated treatment has not been well deciphered. Here, by giving a single dose of APAP (500 mg/kg) to wild-type male mice, combined with a single dose of 500 mg/kg NAC or 100 mg/kg MLT separately as the therapeutic method, this study aimed to investigate the effects of NAC and melatonin (MLT) alone or combined on acetaminophen (APAP)-induced liver injury. In this study, NAC and MLT both partially have an alleviated function in APAP-challenged liver injury. However, MLT's add-on role strengthens the hepatoprotective effect of NAC on APAP-induced liver damage and resolute the inflammatory infiltration. Meanwhile, the combination of two reagents attenuates the decreased glutathione (GSH) and activation of the p38/JNK pathway. The combination of MLT and NAC can further ameliorate APAP-induced liver injury, which provides a novel strategy for drug-induced liver injury (DILI). [ABSTRACT FROM AUTHOR]

Copyright of Anales de Psicología is the property of Servicio de Publicaciones de la Universidad de Murcia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

For at least 50 years, the prevailing view has been that the adenylate cyclase (AC)/cyclic AMP (cAMP)/protein kinase A pathway is the predominant signal mediating the hepatic glucose‐mobilizing actions of glucagon. A wealth of evidence, however, supports the alternative, that the operative signal most of the time is the phospholipase C (PLC)/inositol‐phosphate (IP3)/calcium/calmodulin pathway. The evidence can be summarized as follows: (1) The consensus threshold glucagon concentration for activating AC ex vivo is 100 pM, but the statistical hepatic portal plasma glucagon concentration range, measured by RIA, is between 28 and 60 pM; (2) Within that physiological concentration range, glucagon stimulates the PLC/IP3 pathway and robustly increases glucose output without affecting the AC/cAMP pathway; (3) Activation of a latent, amplified AC/cAMP pathway at concentrations below 60 pM is very unlikely; and (4) Activation of the PLC/IP3 pathway at physiological concentrations produces intracellular effects that are similar to those produced by activation of the AC/cAMP pathway at concentrations above 100 pM, including elevated intracellular calcium and altered activities and expressions of key enzymes involved in glycogenolysis, gluconeogenesis, and glycogen synthesis. Under metabolically stressful conditions, as in the early neonate or exercising adult, plasma glucagon concentrations often exceed 100 pM, recruiting the AC/cAMP pathway and enhancing the activation of PLC/IP3 pathway to boost glucose output, adaptively meeting the elevated systemic glucose demand. Whether the AC/cAMP pathway is consistently activated in starvation or diabetes is not clear. Because the importance of glucagon in the pathogenesis of diabetes is becoming increasingly evident, it is even more urgent now to resolve lingering uncertainties and definitively establish glucagon's true mechanism of glycemia regulation in health and disease. [ABSTRACT FROM AUTHOR]

Previous studies found that seawater immersion combined with hemorrhagic shock (SIHS) induced serious organ function disorder, and lethal triad was a critical sign. There were no effective treatments of SIHS. Fluid resuscitation was the initial measurement for early aid following hemorrhagic shock, while the proper fluid for SIHS is not clear. Effects of different osmotic pressures [lactated Ringer's (LR) solution, 0.3% saline, 0.6% saline, and 0.9% normal saline] on the lethal triad, mitochondrial function, vital organ functions, and survival were observed following SIHS in rats. The results showed that SIHS led to an obvious lethal triad, which presented the decrease of the body temperature, acidosis, and coagulation functions disorder in rats. Fluid resuscitation with different osmotic pressures recovered the body temperature and corrected acidosis with different levels; effects of 0.6% normal saline were the best; especially for the coagulation function, 0.6% normal saline alleviated the lethal triad significantly. Further studies showed that SIHS resulted in the damage of the mitochondrial function of vital organs, the increase of the vascular permeability, and, at the same time, the organ function including cardiac, liver, and kidney was disordered. Conventional fluid such as LR or 0.9% normal saline could not improve the mitochondrial function and vascular leakage and alleviate the damage of the organ function. While moderate hypotonic fluid, the 0.6% normal saline, could lighten organ function damage via protecting mitochondrial function. The 0.6% normal saline increased the left ventricular fractional shortening and the left ventricular ejection fraction, and decreased the levels of aspartate transaminase, alanine transferase, blood urea nitrogen, and creatinine in the blood. The effects of fluids with different osmotic pressures on the mean arterial pressure (MAP) had a similar trend as above parameters. The survival results showed that the 0.6% normal saline group improved the survival rate and prolonged the survival time, the 72 h survival rate was 7/16, as compared with the LR group (3/16). The results indicate that appropriate hypotonic fluid is suitable after SIHS, which alleviates the lethal triad, protects the mitochondrial function and organ functions, and prolongs the survival time. [ABSTRACT FROM AUTHOR]

The influence of methyl jasmonate (MJ) preharvest treatment was investigated on some polyphenols and antioxidant systems in the "Thompson Seedless" table grape. The clusters were sprayed in the vineyard 2 days before harvest with 0, 1, 5, and 10 mM MJ. After picking, berries were stored for 6 days at 15°C, simulating marketing conditions. Total phenols and flavonoids were affected by MJ treatment, especially at 10 mM concentration, whereas total tannins were found to be unchanged. Antioxidant activity of the treated skin was noticeably higher compared with the control, together with PAL and POD activity. Although MJ had little effect on catechin and epicatechin, the levels of quercetin and rutin were noticeable. In addition, 5 and 10 mM MJ exerted a pronounced effect on transresveratrol content. These data showed that a single preharvest application close to the harvest time could be an effective treatment to promote the antioxidant properties of the grape. [ABSTRACT FROM AUTHOR]

Natural products are in great demand because certain secondary metabolites (SMs) are sources of antioxidants, flavorings, active substances, or anticancer agents with less aggressiveness and selectivity, among which triterpenes and flavonoids are of importance because they inhibit carcinogenesis. For Sechium spp. P. Br. (chayotes), there is scientific evidence of antiproliferative activity that has occurred when cancer cell lines have been treated with this fruit. In order to compare future therapeutic designs and identify new and ancestral characteristics, triterpenes and flavonoids were determined in contrasting Sechium genotypes. The obtained data were analyzed via a cladistics approach, with the aim of identifying the characteristics and state of phytochemicals and genetic variables. The concentrations of flavonoids and triterpenes were determined, and a more complex composition of secondary metabolites was found in the wild types as compared to their domesticated genotypes. Bitter fruits contained a higher number of SMs, followed by those with a neutral and sweet flavor. A cladogram showed the differentiation of the three groups based on the flavor of the fruits. The diversity of SMs decreases in evolutionary terms, in response to domestication and environmental adaptation. Therefore, genotypes can be feasibly selected based on fruit flavor for gross-breeding, and cytotoxicity can be reduced without losing possible therapeutic effects. [ABSTRACT FROM AUTHOR]

The whole liver transplantation is the most effective treatment for end-stage fibrosis. However, the lack of available donors, immune rejection and total cost of surgery remain as the key challenges in advancing liver fibrosis therapeutics. Due to the multi-differentiation and low immunogenicity of stem cells, treatment of liver fibrosis with stem cells has been considered as a valuable new therapeutic modality. The pathological progression of liver fibrosis is closely related to the changes in the activities of intrahepatic cells. Damaged hepatocytes, activated Kupffer cells and other inflammatory cells lead to hepatic stellate cells (HSCs) activation, further promoting apoptosis of damaged hepatocytes, while stem cells can work on fibrosis-related intrahepatic cells through relevant transduction pathways. Herein, this article elucidates the phenomena and the mechanisms of the crosstalk between various types of stem cells and intrahepatic cells including HSCs and hepatocytes in the treatment of liver fibrosis. Then, the important influences of chemical compositions, mechanical properties and blood flow on liver fibrosis models with stem cell treatment are emphasized. Clinical trials on stem cell-based therapy for liver fibrosis are also briefly summarized. Finally, continuing challenges and future directions of stem cell-based therapy for hepatic fibrosis are discussed. In short, stem cells play an important advantage and have a great potential in treating liver fibrosis by interacting with intrahepatic cells. Clarifying how stem cells interact with intrahepatic cells to change the progression of liver fibrosis is of great significance for a deeper understanding of liver fibrosis mechanisms and targeted therapy., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)